glucuronidi

Glucuronidi, known in English as glucuronides, are a class of chemical conjugates formed by the attachment of glucuronic acid to a wide range of substrates. They arise mainly through the activity of UDP-glucuronosyltransferases (UGTs), a family of enzymes that transfer glucuronic acid from UDP-glucuronic acid to nucleophilic sites on substrates such as hydroxyl, carboxyl, amine, and sulfur atoms. Glucuronidi can be classified as O-glucuronides, N-glucuronides, S-glucuronides, or acyl glucuronides, depending on the linkage formed.

The primary purpose of glucuronidation is to increase the water solubility of substrates, facilitating their elimination from the body. Most glucuronidi are excreted in bile or urine. The liver is the principal site of glucuronidation, but processes in the intestines, kidneys, and other tissues also contribute. Endogenous substrates include bilirubin, steroid hormones, bile acids, and fatty acids, while many xenobiotics and drugs undergo glucuronidation, such as morphine, acetaminophen, and various nonsteroidal anti-inflammatory drugs.

Glucuronidi formation has significant pharmacological and clinical implications. It influences drug half-life, dose requirements, and potential drug–drug interactions. Impairment of glucuronidation, whether due to genetic variants, disease, or drug inhibition, can lead to accumulation of substrates and associated toxicity. Notable clinical examples include Gilbert and Crigler–Najjar syndromes, which involve reduced bilirubin glucuronidation.

In summary, glucuronidi are detoxification-related metabolites produced by glucuronidation, playing a central role in the metabolism and excretion of many endogenous compounds and xenobiotics.